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Titolo:
Identification of epistatic interactions involved in non-insulin-dependentdiabetes mellitus in the Otsuka Long-Evans Tokushima Fatty rat
Autore:
Yamada, T; Miyake, T; Sugiura, K; Narita, A; Wei, K; Wei, SW; Moralejo, DH; Ogino, T; Gaillard, C; Sasaki, Y; Matsumoto, K;
Indirizzi:
Univ Tokushima, Sch Med, Inst Anim Experimentat, Tokushima 7708503, Japan Univ Tokushima Tokushima Japan 7708503 imentat, Tokushima 7708503, Japan Kyoto Univ, Grad Sch Agr, Lab Anim Breeding & Genet, Kyoto 6068502, Japan Kyoto Univ Kyoto Japan 6068502 im Breeding & Genet, Kyoto 6068502, Japan Univ Bern, Inst Anim Breeding, CH-3012 Bern, Switzerland Univ Bern Bern Switzerland CH-3012 m Breeding, CH-3012 Bern, Switzerland
Titolo Testata:
EXPERIMENTAL ANIMALS
fascicolo: 2, volume: 50, anno: 2001,
pagine: 115 - 123
SICI:
1341-1357(200104)50:2<115:IOEIII>2.0.ZU;2-6
Fonte:
ISI
Lingua:
ENG
Soggetto:
QUANTITATIVE TRAIT LOCI; GENETIC-MAP; SUSCEPTIBILITY; MICE; MUTATIONS; HYPERGLYCEMIA; ALLELES; MOUSE; COLON;
Keywords:
epistasis; genetic dissection; NIDDM; OLETF rat;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Agriculture,Biology & Environmental Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Matsumoto, K Univ Tokushima, Sch Med, Inst Anim Experimentat, Tokushima 7708503, Japan Univ Tokushima Tokushima Japan 7708503 shima 7708503, Japan
Citazione:
T. Yamada et al., "Identification of epistatic interactions involved in non-insulin-dependentdiabetes mellitus in the Otsuka Long-Evans Tokushima Fatty rat", EXP ANIM, 50(2), 2001, pp. 115-123

Abstract

The Otsuka Long-Evans Tokushima Fatty (OLETF) rat is an animal model for obese-type non-insulin-dependent diabetes mellitus (NIDDM) in humans. Our present investigation was designed to identify epistatic interactions influencing NIDDM by performing least squares analysis of variance of all pairs ofinformative markers in 160 F, progenies bred from an intercross of OLETF and Fischer-344 rats. We identified four interactions between Nidd15/of (chromosome 7) and Nidd16/of (chromosome 14), Nidd15/ of and Nidd17/of (chromosome 15), Nidd16/of and Nidd18/of (chromosome 15), and Nidd16/of and Nidd19/of (chromosome 17), which account for a total of similar to 40% of the genetic variation of entire glucose levels after glucose challenge in the F,. The Nidd16/of locus, which is involved in three of four digenic interactions, and the Nidd19/of are likely to correspond to Nidd2/of and Nidd14/of, NIDDM loci previously identified in the F, by single-QTL model and multiple-QTL model, respectively, while Nidd15/of, Nidd17/of and Nidd18/of loci reflect novel NIDDM loci. An aberrant increase of the entire glucose level due tosynergism occurs in the double OLETF homozygote genotype of Nidd15/of and Nidd16/of, and of Nidd16/of and Nidd19/of, as well as in the OLETF homozygote genotypes of Nidd15/ of and Nidd16/of, respectively, combined with the heterozygote genotypes of Nidd17/of and Nidd18/of. These findings demonstrate that inter-allelic interactions are likely to be an important component of NIDDM susceptibility.

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Documento generato il 29/09/20 alle ore 09:44:44